Objective(s): Ceftriaxone (Cef), a beta-lactam antibiotic, is accompanied by antioxidant and antiinflammatory properties. It has been shown that Cef has beneficial effects on Alzheimer’ s disease. In the current investigation, the effect of Cef in a mice model of aging was investigated. Materials and Methods: Forty male mice were equally aliquoted into four groups as follows: Control (as healthy normal animals), D-galactose (DG) group (treated with 500 mg/kg/day DG for 6 weeks), DG + Cef group (treated with DG plus Cef 200 mg/kg/day for 6 weeks), and Cef group (treated with Cef 200 mg/kg/ day for 6 weeks). A battery of behavioral tests was done to evaluate age-related neurocognitive changes. The activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD), as well as the level of malondialdehyde (MDA) in the brain, were measured by biochemical methods. Also, to determine the brain damage, histopathological alterations in the hippocampus were measured using hematoxylin and eosin (H&E) staining. Results: Our results indicate that neurobehavioral dysfunctions of DG can be prevented by coadministration of Cef. We also found that Cef increases the activity of SOD, GPx, and CAT as well as decreasing the level of MDA in the brain of aged mice. Conclusion: Based on our findings, Cef declines neurocognitive dysfunctions in the DG-induced model of aging, possibly through its antioxidative properties.

Objective: Aging is a multifactorial phenomenon, which attribute to different diseases and abnormalities in living systems. Oxidative stress, which is an important factor in aging, exacerbates this process via different mechanisms. Crocin (CR), one of the active components of saffron showed strong antioxidant effects. In the present study, anti-aging property of crocin was investigated in mice. Materials and Methods: The model of aging was induced using administration of d-galactose (500 mg/kg, s. c. ) for 42 days. Animals were treated with crocin (10, 20, 40 mg/kg, i. p. ) during treatment with d-galactose. At the end of treatment, levels of malondialdehyde (MDA) as a lipid peroxidation marker and glutathione content (GSH) in the liver and brain were measured. Also, biochemical factors including liver enzymes (ALT and AST), male sex hormones including testosterone and dehydroepiandrosterone-sulfate (DHEA-SO4) and pro-inflammatory markers such as tumor necrosis factor-α (TNF-α ) and interlukine-6 (IL-6) in serum, were evaluated. Results: Administration of d-galactose led to induction of lipid peroxidation in liver and brain tissues, as well as elevation of AST, ALT, and pro-inflammatory cytokines and reduction of male sex hormones levels in serum. Interestingly, treatment of animals with crocin (10, 20 and 40 mg/kg) diminished lipid peroxidation in the liver and brain tissues while elevated GSH content. Also, a decline in serum levels of TNF-α and IL-6 and an elevation of male sex hormones were observed following treatment with crocin. Conclusion: Administration of crocin reduced d-galactose-induced aging in mice through inhibition of oxidative stress, reduction of inflammation and elevation of sex hormones.

Background: Aging is considered as a gradual biological process, which induces alteration in biochemistry and morphology of a biological system. Thymoquinone (TQ), is the major ingredient of volatile oil from Nigella sativa L. seeds. Because of the various pharmacological effects of TQ, this constituent was used for the current study. Objectives: Anti-aging property of TQ in D-galactose-induced model of aging was investigated in mice. Methods: Aging was induced in Razi mice with D-galactose injection (500 mg/kg, SC, daily) for 42 consecutive days. Animal treatment conducted with D-galactose alone or with different doses of TQ (2. 5, 5 and 10 mg/kg). Malondialdehyde (MDA) and glutathione (GSH) concentrations were determined in liver and brain tissues at the end of treatment. Serum concentration of interleukin 6 (IL-6) and tumor necrosis factor- (TNF- ), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as well as dehydroepiandrosterone-sulfate (DHEA-S) and testosterone were determined. Results: Administration of D-galactose (500 mg/kg, SC, daily) for 42 consecutive days increased the level of MDA in brain and liver tissues while diminished the GSH content. Additionally, the serum levels of TNF- , IL-6, ALT and AST were significantly elevated following induction of aging phenomena while the level of male sex hormones were markedly reduced. Treatment with TQ (5 and 10 mg/kg) elevated level of GSH while decreased MDA production. In addition, the serum level of TNF- , IL-6, ALT and AST decreased while the level of male sex hormones improved following treatment with TQ. Conclusions: TQ showed anti-aging effect in this model. These effects in part can be mediated through antioxidant effects of TQ.

Objective(s): Metformin (Met), an antidiabetic biguanide, reduces hyperglycemia via improving glucose utilization and reducing the gluconeogenesis. Met has been shown to exert neuroprotective, antioxidant and anti-inflammatory properties. The present study investigated the possible effect of Met on the D-galactose (D-gal)-induced aging in mice. Materials and Methods: Met (1 and 10 mg/kg/p. o. ), was administrated daily in D-gal-received (500 mg/kg/p. o. ) mice model of aging for six weeks. Anxiety-like behavior, cognitive function, and physical power were evaluated by the elevated plus-maze, novel object recognition task (NORT), and forced swimming capacity test, respectively. The brains were analyzed for the level of superoxide dismutase (SOD) and brain-derived neurotrophic factor (BDNF). Results: Met decreased the anxiety-like behavior in D-gal-treated mice. Also, Met treated mice showed significantly improved learning and memory ability in NORT compared to the D-gal-treated mice. Furthermore, Met increased the physical power as well as the activity of SOD and BDNF level in D-gal-treated mice. Conclusion: Our results suggest that the use of Met can be an effective strategy for prevention and treatment of D-gal-induced aging in animal models. This effect seems to be mediated by attenuation of oxidative stress and enhancement of the neurotrophic factors.

Background & Objective: Aging is a natural phenomenon which can cause changes in most organs and cells. Numerous mechanisms including oxidative stress and free radical generation is involved in the progression of the aging process. Pomegranate seed oil (PSO), has different therapeutic properties including anti-oxidant and anti-inflammatory effects. In this research, the effect of PSO against D-galactose-induced aging is investigated. Materials & Methods: D-galactose, 500 mg/kg, injected subcutaneously (S. C. ) to induce aging in rats. Animals in treatment groups received PSO, 0. 4 and 0. 8 ml/kg intraperitoneally (i. p. ). After 42 days, behavioral test was evaluated by passive avoidance (PA). Then animals killed, blood samples collected by cardiac puncture, and brain and liver removed. Levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) measured in serum. Malondialdehyde (MDA) and thiol contents of brain and liver homogenized tissue samples were determined. Results: D-galactose increased lipid-peroxidation in liver and brain tissues as well as elevation of ALT, AST, but the level of thiol contents decreased in homogenized tissues. Both doses of PSO attenuated d-galactose-induced injury in liver and brain by decreasing ALT, AST, MDA and elevation of thiol content. The PA test showed that PSO increased the latency time to enter the dark chamber compared to the control group. Conclusion: PSO decreased D-galactose-induced aging in rats via prevention of oxidative stress. This effect may be related to the presence of various compounds and their anti-oxidant properties, which is found in PSO.

Aging is a progressive process which is associated with liver dysfunction and it is due to oxidative stress, inflammation, and cell apoptosis. Long-term D-galactose (D-gal) administration is able to develop an aging model in animals. Crocin as a major active ingredient in saffron has shown anti-inflammatory and hepatoprotective effects via its antioxidant capacity. Thus, the aim of the present study was the assessment of crocin effects on hepatic and metabolic disorders induced by D-gal in rats. Aging model was induced in rats by 56-day administration of D-gal (400 mg/kg/day subcutaneously). Protective effects of different doses of crocin (7. 5, 15 and 30 mg/kg/day) in concomitant with D-gal administration were evaluated. Malondialdehyde (MDA) and reduced glutathione (GSH) amounts were measured by means of their reaction, respectively, with thiobarbituric acid and 5, 5′-Dithiobis (2-nitrobenzoic acid) (DTNB) under a specific condition. Cyclooxygenase-2 (COX-2), β-galactosidase, induced nitric oxide synthase (iNOS), and carboxymethyllysine (CML) levels were determined by western blotting method. Additionally, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured in serum. D-gal administration significantly elevated ALT, AST, ALP levels, which were markedly inhibited by crocin administration. Crocin suppressed the overgeneration of lipid peroxidation products such as MDA. iNOS was elevated by D-gal administration and was returned to the normal extent by crocin. Therefore, Crocin as a powerful antioxidant and radical scavenger, totally exhibited hepatoprotective effects against D-gal-induced toxicity in rats.